Vetiver oil (Java) attenuates cisplatin-induced oxidative stress, nephrotoxicity and myelosuppression in Swiss albino mice. (July 2015)

• Record Type: Journal Article
• Authors: Sinha, Sonali; Jothiramajayam, Manivannan; Ghosh, Manosij; Jana, Aditi; Chatterji, Urmi; Mukherjee, Anita
• Is Part Of: Food and chemical toxicology. Volume 81(2015)
• Page Start: 120
• Page End: 128
• Publication Date: 2015-07
• Subjects: Cisplatin -- Vetiver acetate oil -- Oxidative stress -- Nephrotoxicity -- Genotoxicity -- Myelosuppression; Toxicology -- Periodicals; Food poisoning -- Periodicals; Food Poisoning -- Periodicals; Toxicology -- Periodicals; Toxicologie -- Périodiques; Intoxications alimentaires -- Périodiques; Food poisoning; Toxicology; Periodicals; Electronic journals; 615.9
• DOI: 10.1016/j.fct.2015.04.018
• Languages: English
• ISSNs: 0278-6915

Abstract

Highlights: Significant amelioration of cisplatin-induced toxicity in normal tissues was achieved by priming Swiss albino mice with VO. Mitigation of nephrotoxicity was evident from reduced levels of serum BUN, creatinine and renal oxidative stress markers. VO mitigated genotoxicity in both renal and bone marrow cells, reduced myelosuppression and hematotoxicity. VO at dose of 5 mg/kg bw was most effective. VO can be a potential drug for adjuvant therapy. Graphical Abstract: Abstract: Clinical efficacy of the widely used anticancer drug cisplatin is limited due to its adverse side effects in normal tissues mediated by oxidative stress. This study was aimed to investigate the protective effects of vetiver acetate oil, Java (VO) against cisplatin-induced toxicity in Swiss albino mice. The ameliorating potential was evaluated by orally priming the animals with VO at doses 5, 10 or 20 mg/kg bw for 7 days prior to cisplatin treatment. Acute toxicity in mice was induced by injecting cisplatin (3 mg/kg bw) intraperitoneally for 5 consecutive days. Significant attenuation of renal toxicity was confirmed by histopathological examination, lowered levels of serum blood urea nitrogen, creatinine and reduced DNA damage. VO also compensated deficits in the renal antioxidant system. VO intervention significantly inhibited DNA damage, clastogenic effects, and cell cycle arrest in the bone marrow cells of mice. Hematological parameters indicated attenuation of cisplatin-induced myelosuppression. Overall, this study provides for the first time that VO has a protective role in the abatement of cisplatin-induced toxicity in mice which may be attributed to its antioxidant activity.